The release of platelet factor 4 (PF4) from platelets in platelet concentrates (PC) were investigated sequentially in the process of blood collection, and their storage at room temperature for up to 72h with agitation. No appreciable increase in PF4 release was seen immediately after blood collection. However, after resuspension of pelleted platelets with platelet-poor plasma, a significant increase in PF4 release appeared without increase in extracellular lactic dehydrogenase (LDH) concentrations in PC. After storage for 24h, PF4 release was positively correlated with LDH leakage. Approximately 41% of the total amount of PF4 was observed in supernatants in PC after storage for 3 days, while LDH leakage was less than 3% of the total amount in platelets. Rates of pH fall were roughly proportional to the platelet count, and there was positive relationship between PF4 release and the platelet count.
We conclude that storage of platelets under the pelleted condition and resuspension with platelet-poor plasma with the aid of an agitator are critical for better maintenance of PF4 in platelets, and lowering the platelet concentration in the storage bag may prevent release of α-granular constituents in great amounts.

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Blood gases of platelet concentrates (PC) were measured at 37°C by means of a pH/gas analyzer. About 19ml of PC were stored in a 150ml storage bag made of polyvinyl chloride with flat-bed agitation at 22°C for up to 3 days. PC pH fall was roughly proportional to the platelet count, in which the CO₂ tension was inversely associated with the O₂ tension. Rates of pH fall were due to not only lactate generation by platelet anerobic glycolysis but an increase in CO₂ tension. The relationship between PC pH and the platelet count was maintained during 3-day storage, although the CO₂ tension but not the O₂ tension decreased significantly on day 3 with increasing production rates of lactate. The present results indicate that PC with a higher platelet count become acidified during storage, and one beneficial way to prevent this pH fall is solely to lower the platelet concentration in the storage bag.

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An example of anti-K1 found in a Japanese patient with occipitalcraniomenigiomata, aged 19 years, is reported. His red cells had not K1 antigen. The patient had no history of prior blood transfusion, but he received twelve units of K1 negative and compatible red blood cells at the time of surgery in July 1982. No clinical and haematological signs of red cell destruction were noted. Unexpected antibodies were not detectable by routine pretransfusion screening.
However, in September 1982, his serum was found to contain an IgG antibody with anti-K (K1) specificity; the titer of which was 16 to 32 with K:1 and 8 to 16 with K:1, 2 cell samples by the indirect antiglobulin test using anti-IgG.
His red cells gave a doubtful direct antiglobulin test using polyspecific antiglobulin and anti-C3, but not anti-IgG. Anti-K1 specificity was demonstrated in an eluate from his red blood cells.
The antibody stimulation of the anti-K1 remains unknown.

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Three techniques for the preparation of leukocyte poor red blood cell concentrates are described. The final step of each technique amploys microaggregate blood filtration to remove large quantities of aggregated white cells from the blood. The first technique, microaggregated blood filtration alone, removes 67% of the leukocytes from stored blood. The second procedure, high speed centrifugation followed by microaggregate filtration, eliminates 83% of the WBC. The final technique, centrifugation followed by 3 hours of refrigeration and filtration, removes >85% of the leukocytes from fresh blood. The efficiency of each technique varies directly with the unit's storage age. The red cell loss imposed by these procedures averages >8%. Transfusion of the products produced by these procedures was shown to reduce the likelihood of febrile transfusion reactions by as much as 40-fold. The techniques offer several advantages over those procedures, currently used to produce leukocyte poor blood, viz. cost effectiveness, “closed system processing”, ready availability, and red cell conservation.

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When only pressures and flow are examined, but not oxygen transport and oxygen consumption, crystalloids may appeart to be satisfactory, particularly in the elective patient who is not in shock. Body water shifts after hemorrhage, trauma and various combinations of these; proponents of the crystalloid school of thought believe reduced interstitial water (ISW) is the major problem in both hemorrhage and trauma, while others, who question the validity of ³⁵SO₄ as a measure of ISW, believe that the primary circulatory problem is hypovolemia. Sodium is known to increase arterial pressure and urine output; if these effects are used to test therapeutic efficacy; then sodium-rich solutions will be found to be effective even though they do not correct the essential defect of shock and trauma states.
Fluid shifts have been described as either a “leak” or “equilibration” of the administered fluids according to the viewpoint of the observer. Irrespective of these interpretations, the net water shift in or out of the plasma volume has been measured before and after fluid therapy. In essence, crystalloids expand the ISW, as over 80% leaves the plasma before the end of the infusion; bu contrast, albumin increases plasma volume particularly in the early postoperative course of critically ill surgical patients. Blood volume expansion with massive volumes of crystalloids by virtue of the associated massive interstitial water expansion, may improve plasma volume, but this may also impede peripheral oxygen diffusion and worsen tissue oxygenation. In the postoperative shock patient, and the patient in early ARDS, blood volume and oxygen delivery are more effectively provided by colloids.
Pulmonary edema may result from cardiogenic factors, noncardiac (ARDS) factors and excessive fluid administration. Salt and water restriction, diuretics and other supportive measures are usually indicated. When pulmonary edema is associated with hypovolemia, concentrated (25%) albumin may restore body water distribution by shifting fluid from the interstitium into the plasma volume. However, when pulmonary edema is due to interstitial pneumonitis, viral pneumonia and other medical causes of respiratory failure, the pulmonary capillay-alveolar membrane leak which usually occurs in the late stage of ARDS may be worsened by colloid therapy.
Irrespective of philoscophical considerations of protagonists of a “partyline”, the critically ill, high risk patinnt should be monitored with sophisticated hemodynamic and O₂ transport measurements in order to optimize the values of these variables to achieve maximum chances of survival.

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